In order to determine the rate and magnitude of respiratory O-2 depletion during dives of emperor penguins (Aptenodytes forsteri), air sac O-2 partial pressure (PO2) was recorded in 73 dives of four birds at an isolated dive hole. These results were evaluated with respect to hypoxic tolerance, the aerobic dive limit (ADL; dive duration beyond which there is post-dive lactate accumulation) and previously measured field metabolic rates (FMRs). 55% of dives were greater in duration than the previously measured 5.6-min ADL. P-O2 and depth profiles revealed compression hyperoxia and gradual O-2 depletion during dives. 42% of final P(O2)s during the dives (recorded during the last 15 s of ascent) were < 20 mmHg (< 2.7 kPa). Assuming that the measured air sac P-O2 is representative of the entire respiratory system, this implies remarkable hypoxic tolerance in emperors. In dives of durations greater than the ADL, the calculated end-of-dive air sac O-2 fraction was < 4%. The respiratory O-2 store depletion rate of an entire dive, based on the change in O-2 fraction during a dive and previously measured diving respiratory volume, ranged from I to 5 ml O-2 kg(-1) min(-1) and decreased exponentially with diving duration. The mean value, 2.1 +/- 0.8 ml O-2 kg(-1) min(-1), was (1) 19-42% of previously measured respiratory O-2 depletion rates during forced submersions and simulated dives, (2) approximately one-third of the predicted total body resting metabolic rate and (3) approximately 10% of the measured FMR. These findings are consistent with a low total body metabolic rate during the dive.

H-1 NMR solution-state study of elephant seal (Mirounga angustirostris) myoglobin (Mb) and hemoglobin (Hb) establishes the temperature-dependent chemical shifts of the proximal histidyl NdeltaH signal, which reflects the respective intracellular and vascular PO2 in vivo. Both proteins exist predominantly in one major isoform and do not exhibit any conformational heterogeneity. The Mb and Hb signals are detectable in M. angustirostris tissue in vivo. During eupnea M. angustirostris muscle maintains a well-saturated MbO(2). However, during apnea, the deoxymyoglobin proximal histidyl NdeltaH signal becomes visible, reflecting a declining tissue PO2. The study establishes a firm methodological basis for using NMR to investigate the metabolic responses during sleep apnea of the elephant seal and to secure insights into oxygen regulation in diving mammals.

The emperor penguin (Aptenodytes forsteri) thrives in the Antarctic underwater environment, diving to depths greater than 500m and for durations longer than 23 min. To examine mechanisms underlying the exceptional diving ability of this species and further describe blood oxygen (O(2)) transport and depletion while diving, we characterized the O(2)-hemoglobin (Hb) dissociation curve of the emperor penguin in whole blood. This allowed us to (1) investigate the biochemical adaptation of Hb in this species, and (2) address blood O(2) depletion during diving, by applying the dissociation curve to previously collected partial pressure of O(2) (P(O2)) profiles to estimate in vivo Hb saturation (S(O2)) changes during dives. This investigation revealed enhanced Hb-O(2) affinity (P(50)=28mmHg, pH7.5) in the emperor penguin, similar to high-altitude birds and other penguin species. This allows for increased O(2) at low blood P(O2) levels during diving and more complete depletion of the respiratory O(2) store. S(O2) profiles during diving demonstrated that arterial S(O2) levels are maintained near 100% throughout much of the dive, not decreasing significantly until the final ascent phase. End-of-dive venous S(O2) values were widely distributed and optimization of the venous blood O(2) store resulted from arterialization and near complete depletion of venous blood O(2) during longer dives. The estimated contribution of the blood O(2) store to diving metabolic rate was low and highly variable. This pattern is due, in part, to the influx of O(2) from the lungs into the blood during diving, and variable rates of tissue O(2) uptake.